Mitochondrial Ca2+ transport, permeability transition and oxidative stress in cell death: implications in cardiotoxicity, neurodegeneration and dyslipidemias (original) (raw)
Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Mitochondrial Ca2+ transport, permeability transition and oxidative stress in cell death: implications in cardiotoxicity, neurodegeneration and dyslipidemias
Anibal E Vercesi 1,*, Alicia J Kowaltowski 2, Helena C F Oliveira 3, Roger F Castilho 1
1 Departamento de Patologia Clinica, Faculdade de Ciencias Medicas, Universidade Estadual de Campinas, Campinas, SP, 13083-970, Brazil
2 Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo, SP, 05508-900, Brazil
3 Departamento de Fisiologia e Biofisica, Instituto de Biologia, Universidade Estadual de Campinas, Campinas, SP, 13083-970, Brazil
Abstract
Mitochondrial Ca2+ transport is important in the maintenance of intracellular ion homeostasis, and also a key factor in the pathogenesis of many diseases. We discuss here the main aspects of mitochondrial Ca2+ transport, and how this transport is linked to changes in energy metabolism and redox state. Mitochondrial permeability transition, a consequence of excessive mitochondrial Ca2+ accumulation associated with oxidative stress is also discussed. Finally, our current understanding of the involvement of these mitochondrial processes in cardiac ischemia-reperfusion, neurodegeneration and dyslipidemias is presented.
Keywords
- Mitochondria
- Calcium
- Potassium
- Free Radicals
- Apoptosis
- Necrosis
- Stroke
- Heart Attack
- Dyslipidemia
- Review